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Developmental Effects of Intrauterine and Lactational Exposure to Nanoplastics and Phthalates on Rat Testis
Summary
A new study found that when pregnant rats were exposed to nanoplastics and phthalates (chemicals found in plastics), their male offspring showed lasting damage to testicle development, including changes to sperm-producing cells and increased oxidative stress that persisted into adulthood. The combination of both chemicals caused more harm than either one alone, suggesting that real-world exposure to multiple plastic-related pollutants during pregnancy could pose bigger risks to male reproductive health than scientists previously realized—though more research is needed to confirm these effects translate to humans.
The toxicity of nanoplastics (NPs) and plastic additives such as phthalates, recognized endocrine-disrupting chemicals, remains insufficiently understood, particularly regarding their combined effects on male reproductive health across the lifespan. Since these contaminants can cross biological barriers, including the placenta, this study, grounded in the developmental origins of health and disease (DOHaD) concept, evaluated the effects of gestational and lactational exposure to NPs and a phthalate mixture (PM) on testicular development and function in male offspring. Pregnant SD rats were allocated to six groups: control (CTRL); T1 (20μg/kg/day PM); T2 (200mg/kg/day PM); T3 (NPs: 1mg/kg/day,100nm); T4 (20μg/kg/day PM+NPs); and T5 (200mg/kg/day PM+NPs). Animals were exposed orally from gestational day 10 to postnatal day (PND)21. Male offspring were euthanized at PND22 (prepuberty) and PND120 (adulthood). At PND22, increased apoptosis in pachytene spermatocytes was observed in the T5 group compared with the CTRL, along with altered gene expression, including increased Amh (T4 vs.T1) and Srd5a1 (T1-T4 vs.CTRL) and reduced Ar expression (T3 vs.CTRL). At PND120, the exposure decreased seminiferous tubule diameter (T2), epithelial height (T1-T5), and numbers of Sertoli (T2-T5) and Leydig cells (T4 and T5) compared to the CTRL. Histopathological alterations were more incident in the T1, T3, T4, and T5 compared to the CTRL, and reduced Tjp1 expression in co-exposed animals suggested impairment of the blood-testis barrier. Redox analyses revealed age-dependent worsening of oxidative stress, particularly in co-exposure groups. Overall, gestational co-exposure to phthalates and NPs disrupts testicular morphology, gene regulation, and redox balance, indicating synergistic and persistent reproductive toxicity.